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The prevalence of persistent hyperglycaemia during diabetes, impair antioxidant defence system and generate reactive oxygen species, which majorly contribute to its progression and associated complications. Phytochemicals were suggested to scavenge‐free radicals and exert antioxidant effects required to improve insulin sensitivity and reduce the occurrence of diabetes‐associated complications. We hypothesise that a phenolic phytochemical p‐coumaric can reduce diabetes‐induced oxidative stress and improve diabetes‐associated nephropathy in rats. The aim of this study is to analyse the protective effects of p‐coumaric acid against diabetes‐induced oxidative stress and nephropathy in high‐fat diet‐induced diabetic rats. The oral feeding of p‐coumaric acid (20 mg/kg for 12 weeks) was found to significantly decrease the elevated levels of blood glucose in high‐fat diet‐induced type 2 diabetic rats. p‐Coumaric acid treatment also decreases the kidney weight whilst increasing the total body weight of diabetic rats. Furthermore whilst evaluation of the different renal functioning tests, p‐coumaric acid significantly improves histopathological changes and the levels of urea, creatinine and uric acid in serum of diabetic rats, which was otherwise elevated under diabetic conditions. Our results also highlight that p‐coumaric acid is an efficient compound with antioxidant properties and improves the diabetes‐induced change in lipid peroxidation and activities of antioxidant enzymes: catalase, glutathione‐S‐transferase and superoxide dismutase. p‐Coumaric acid thus possesses the potential to prevent diabetic nephropathy by reducing oxidative stress and can thus serve as a potential drug target for pharmaceutical companies. [ABSTRACT FROM AUTHOR]

The study aimed to investigate the acute toxicity, antidiabetic potential (in-vitro and in-vivo) of the Operculina turpethum (L.) Silva Manso at fraction level. The plant was fractionated into different fractions, i.e., flavonoid fraction (OTFF), tannin fraction (OTTF), saponin fraction (OTSF). In-vitro alpha-amylase inhibition assay revealed that OTFF was found to be more potent than standard Acarbose. The plant fractions were evaluated by MTT assay at different concentrations ranging from 100 to 1000 µg/ml. All the fractions were further evaluated for their safety profile, and the biochemical, hematology and histopathology result exhibits that the OTFF fraction produces mild toxicity at organ level at a concentration of 2000 mg/kg in albino mice. The in-vivo antidiabetic study was carried out on Sprague-Dawley rats using high-fat diet (HFD) feeding streptozotocin (STZ) diabetic model, and the biochemical, histopathology research findings represent that OTFF at a concentration of 500 mg/kg, p.o. was found to be highly significant among all the fractions and found to be more potent than the standard Acarbose. LC–MS characterization of the bioactive fraction OTFF showed the presence of rutin with m/z 610.52 in 50.50% and Apigenin 7-O-6'' acetyl-glucoside with m/z 475.42 in 24.10%; from molecular docking study, it is predicted that the fraction primarily acts as an alpha-amylase inhibitor and PPAR gamma agonist. In conclusion, the plant's OTFF fraction acts as a potential therapeutic agent for Type II diabetes mellitus. [ABSTRACT FROM AUTHOR]

In the present study, we investigated the anti-Parkinson's effect of vanillic acid (VA) (12 mg/kg, 25 mg/kg, 50 mg/kg p.o.) against rotenone (2 mg/kg s.c.) induced Parkinson's disease (PD) in rats. The continuous administration of rotenone for 35 days resulted in rigidity in muscles, catalepsy, and decrease in locomotor activity, body weight, and rearing behaviour along with the generation of oxidative stress in the brain (rise in the TBARS, and SAG level and reduced CAT, and GSH levels). Co-treatment of VA and levodopa-carbidopa (100 mg/kg + 25 mg/kg p.o.) lead to a significant (P < 0.001) reduction in the muscle rigidity and catalepsy along with a significant (P < 0.001) increase in body weight, rearing behaviour, locomotion and muscle activity as compared to the rotenone-treated group in the dose dependent manner, showing maximum effect at the 50 mg/kg. It also showed reversal of levels of oxidative stress parameters thus, reducing the neuronal oxidative stress. The level of DA was also estimated which showed an increase in the level of DA in the VA plus standard drug treated animals as compared to rotenone treated group. Histopathological evaluation showed a high number of eosinophilic lesions in the rotenone group which were found to be very less in the VA co-treated group. The study thus proved that co-treatment of VA and levodopa-carbidopa, significantly protected the brain from neuronal damage due to oxidative stress and attenuated the motor defects indicating the possible therapeutic potential of VA as a neuroprotective in PD. [ABSTRACT FROM AUTHOR]

• RP-HPLC method for fisetin was developed in rat plasma. • The developed method was validated as per ICH guidelines. • Method was found linear in the concentration range of 25–125 ng/mL. • Recovery above 95% and % RSD less than 2 indicated about accuracy and precision of method. • Absence of interfering peaks at the retention times of fisetin and quercetin indicated method's specificity. Fisetin is an important phyto-flavonoid that possesses very good anti-oxidant, anti-Parkinson's and anti-cancer activities. A bioanalytical method was developed and validated for the estimation of fisetin in the rat's plasma using reverse phase ultra-fast liquid chromatography combined with a C-18 reverse phase column. Quercetin was used as an internal standard. The mobile phase was composed of acetonitrile and orthophosphoric acid (0.2% v/v) in the ratio of 30:70 v/v. Flow rate was set at 1 mL/min and chromatogram of both compounds was detected at a wavelength of 362 nm. Protein precipitation method was used to extract drug from plasma samples. The retention times for fisetin and quercetin were found at 8.3 min and 16.9 min, respectively. The developed method was found to be linear in the range of 25–125 ng/mL with regression coefficient (r 2) of 0.9996. The method was validated as per the ICH Q2 (R1) guidelines. The percentage recovery was in the range of 95–105%, which indicated that method was accurate. The percentage relative standard deviation was found to be less than 2% which indicates that method was precised. Limit of detection (LOD) and limit of quantification (LOQ) were found to be 3.18 ng/mL and 9.66 ng/mL, respectively. The developed method was found to be robust as there was no any significant change in response with change in flow rate and composition of mobile phase. Obtained results indicated that the developed method has passed all the validation test parameters and can be applied successfully for estimation of fisetin in the rat plasma. [ABSTRACT FROM AUTHOR]

Elaeagnus conferta Roxb. (Elaeagnaceae) is a subtropical shrub mainly native to India, Vietnam, Malaysia and South China, whose various parts are used for treatment of diabetes, gastric ulcers, pain, oxidative stress and pulmonary disorders. Though the other parts of the plant have been reported for their ethnic use i.e. fruits as astringent locally and for cancer systemically, leaves for body pain and flowers for pain in chest and the seeds are mentioned as edible, there is no report per se on the medicinal use of seeds. Based on the fact that seeds of closely resembling species i.e. Elaeagnus rhamnoides has demonstrated significant anti-gastroulcerative property, the probability of the seeds of E. conferta possessing similar activity seemed quite significant. Phytochemical investigation and assessment of pharmacological mechanism(s) involved in anti-ulcer effect of methanolic extract of the seeds of E. conferta. Bioactive phytoconstituents were isolated by column chromatography. These were identified by spectroscopic techniques including infrared (IR) spectroscopy, nuclear magnetic resonance (NMR) and mass spectrometry. Methanolic extract (MEC) of the seeds was prepared by cold maceration and its anti-ulcerogenic potential was evaluated using indomethacin (50 mg/kg) and water immersion stress models in male rats. The animals were pre-treated with different doses of MEC (400 and 800 mg/kg) and the therapeutic effect was compared with standard drug i.e. ranitidine (RANT; 50 mg/kg). The ameliorative effects of MEC were investigated on gastric juice pH, total acidity, free acidity and ulcer index. The assays of malionaldehyde (MDA), catalase (CAT), superoxide dismutase (SOD), glutathione (GSH) and pro-inflammatory cytokines i.e. interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were carried out to find out the possible mechanism(s) of protection. Further, histopathological changes were also studied. Chromatography studies and further confirmation by spectroscopic techniques revealed the presence of four different compounds in MEC i.e oleic acid (1), stearic acid (2), ascorbic acid (3) and quercetin (4). MEC exhibited anti-ulcerogenic effect in dose dependent manner which may be attributed to suppression of pro-inflammatory cytokines (IL-6, TNF-α) and MDA (112.7%), and up-regulation of protective factors such as CAT (90.48%), SOD (92.77%) and GSH (90.01%). Ulcer inhibition, reduction in total and free acidity and increase in gastric juice pH were observed in MEC treated rats as compared to disease control animals. Histopathological findings confirmed decreased cell infiltration, less epithelial cell damage and regeneration of gastric mucosa in dose dependent manner. The anti-ulcer effect of MEC may be attributed to its ability to scavenge free radicals and anti-inflammatory property via suppression of TNF-α and IL-6, thus offers a complete and holistic approach for management of peptic ulcer. [Display omitted] • Methanolic extract of Elaeagnus conferta (MEC) suppresses ulcer formation in Wistar rats by altering biochemical parameters. • Gastroprotective effect of MEC is attributed to increase in gastric juice pH, thereby neutralizing gastric acidity. • Structure elucidation of isolated compounds confirmed the presence of oleic acid, stearic acid, ascorbic acid and quercetin. • MEC suppresses ulceration by down-regulating inflammatory mediators i.e. TNF-α and IL-6. • Histopathological findings confirm a decrease in cell infiltration as well as in epithelial cell damage. [ABSTRACT FROM AUTHOR]